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Set point theory does not on its own explain why body mass index for humans, measured as a proxy for fat, tends to change with increasing age or why obesity levels in a population vary depending on socioeconomic or environmental factors (or why weight tends to change for an individual when socioeconomic status and environment change). [4]
Fat mass and obesity-associated protein, also known as alpha-ketoglutarate-dependent dioxygenase FTO, is an enzyme that in humans is encoded by the FTO gene located on chromosome 16. As one homolog in the AlkB family proteins, it is the first messenger RNA (mRNA) demethylase that has been identified. [ 5 ]
Osteoarthritis and obesity are closely linked. Obesity is one of the most important preventable factors for the development of osteoarthritis. Originally, the relationship between osteoarthritis and obesity was considered to be exclusively biomechanically based, according to which the excess weight caused the joint to become worn down more quickly.
Preclinical obesity refers to excess body fat without current health issues but with increased risks of conditions like type 2 diabetes, heart disease, and certain cancers. Early interventions can ...
One study found that 80% of the offspring of two obese parents were obese, in contrast to less than 10% of the offspring of two parents who were of normal weight. [ 30 ] The thrifty gene hypothesis postulates that due to dietary scarcity during human evolution people are prone to obesity.
Obesity is one of the leading preventable causes of death worldwide. [38] [39] [40] The mortality risk is lowest at a BMI of 20–25 kg/m 2 [41] [37] [42] in non-smokers and at 24–27 kg/m 2 in current smokers, with risk increasing along with changes in either direction. [43] [44] This appears to apply in at least four continents. [42]
Sellayah and colleagues have postulated an 'Out of Africa' theory to explain the evolutionary origins of obesity. The theory cites diverse ethnic based differences in obesity susceptibility in western civilizations to contend that, neither the thrifty or drifty gene hypotheses can explain the demographics of the modern obesity crisis.
By studying mice and tumour samples from kidney cancer patients, they found that obesity increases the number of macrophages in cancer tumours and increases their production of a protein called PD 1.